Access

You are not currently logged in.

Access your personal account or get JSTOR access through your library or other institution:

login

Log in to your personal account or through your institution.

If You Use a Screen Reader

This content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.

Prostaglandins Evoke a Whole Variety of Responses in the Lung

Philip J. Kadowitz, Ernst W. Spannhake and Albert L. Hyman
Environmental Health Perspectives
Vol. 35 (Apr., 1980), pp. 181-190
DOI: 10.2307/3428988
Stable URL: http://www.jstor.org/stable/3428988
Page Count: 10
  • Read Online (Free)
  • Subscribe ($19.50)
  • Cite this Item
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Prostaglandins Evoke a Whole Variety of Responses in the Lung
Preview not available

Abstract

Rapid intravenous (IV) injections of the prostaglandin precursor arachidonic acid (AA) increase pulmonary arterial pressure (PAP) and pulmonary vascular resistance (PVR) in a variety of species. It has recently been reported that infusions of AA decrease PAP. The purpose of this report is to contrast responses to bolus injections and infusions of AA in the anesthetized cat. In all experiments rapid IV injections of AA increased PAP and PVR; however, infusions of 68 to 680 μg/min produced variable responses. In 10 of 19 animals, AA infusion decreased PAP and PVR, and this response was enhanced when pulmonary vascular tone was actively increased by vasoconstrictor agents or alveolar hypoxia. In the other nine animals, the predominant response was an increase in PAP and PVR. In all experiments infusions of larger amounts of AA (1.4 to 3.4 mg/min) increased PAP. Both pressor and depressor responses to AA were inhibited by meclofenamate. This study shows that infusion of small amounts of AA dilates or constricts the pulmonary vascular bed. In contrast, infusion of larger amounts of AA always causes vasoconstriction. These data suggest that at low infusion rates, PGI2, which is a vasodilator, is the predominant metabolite formed from AA in some animals. However, at higher concentrations, the production of constrictor products predominates. These experiments also suggest that the products formed and the response observed may be dependent on a number of factors including the amount of tone present in the pulmonary vascular bed.

Page Thumbnails

  • Thumbnail: Page 
181
    181
  • Thumbnail: Page 
182
    182
  • Thumbnail: Page 
183
    183
  • Thumbnail: Page 
184
    184
  • Thumbnail: Page 
185
    185
  • Thumbnail: Page 
186
    186
  • Thumbnail: Page 
187
    187
  • Thumbnail: Page 
188
    188
  • Thumbnail: Page 
189
    189
  • Thumbnail: Page 
190
    190